Antepartum and Postpartum Hemorrhage (PDF)

Antepartum & Postpartum Hemorrhage A S H T O N T. A V E R I T T D N P, CRNA Introduction Obstetric hemorrhage is the most common cause of maternal mortality worldwide, accounting for roughly 15% of maternal deaths. The WHO estimates that severe hemorrhage complicates 10.5% of live births glob...

Antepartum & Postpartum Hemorrhage A S H T O N T. A V E R I T T D N P, CRNA Introduction Obstetric hemorrhage is the most common cause of maternal mortality worldwide, accounting for roughly 15% of maternal deaths. The WHO estimates that severe hemorrhage complicates 10.5% of live births globally and carries with it a case-fatality rate of 1%. The rates of maternal death and death caused by hemorrhage vary widely throughout various regions of the world. In the US, hemorrhage accounts for 11.4% of pregnancy- related deaths (approx. 1.9 per 100,000 live births). Hemorrhage is the most common cause for admission of an obstetric patient to an intensive care unit (ICU) and is a risk factor for myocardial ischemia, infarction, and stroke. Organ dysfunction complicates 16% of cases of OB hemorrhage accompanied by Introduction Hemorrhage and severe morbidity caused by hemorrhage are increasing in the US and other high-resource countries, primarily caused by increases in postpartum, rather than antepartum, hemorrhage. The explanation is not entirely clear but appears to be related to rising rates of postpartum uterine atony as well as increases in abnormal placentation coincident with the rise in cesarean delivery rates. The majority of hemorrhage-related adverse outcomes are considered preventable. Mechanisms of Hemostasis Uterine contraction, stimulated by endogenous oxytocic substances released after delivery, represents the primary mechanism for controlling blood loss at parturition. Uterine tetany creates shearing forces that cleave the placenta from the uterine wall through the later of the uterine decidua. In addition, uterine contraction constricts the spiral arteries and placental veins, spanning the myometrium and supplying the placental bed. After disruption of vascular integrity, mechanisms of coagulation include, (1) platelet aggregation and plug formation, (2) local vasoconstriction, (3) clot polymerization, and (4) fibrous tissue fortification of the clot. Platelet activation and aggregation occur rapidly after endothelial damage. Activated platelets release adenosine diphosphate, serotonin, catecholamines, and other factors that promote local vasoconstriction and hemostasis. These factors also activate the coagulation cascade. The end result of the cascade is the conversion of fibrinogen to fibrin and the stabilization of the clot. Antepartum Hemorrhage Antepartum vaginal bleeding may occur in as many as 25% of pregnant women; fortunately, only a fraction of these patients experience life-threatening hemorrhage. The majority of cases occur during the first trimester. The causes of antepartum hemorrhage range from cervicitis to abnormalities in placentation, including placenta previa and placental abruption. The greatest threat of antepartum hemorrhage is not to the mother but to her fetus. Several decades ago, vaginal bleeding during the second and third trimesters was associated with perinatal mortality rates as high as 80%. More recent data suggests that antepartum bleeding secondary to placenta previa and placental abruption results in far fewer neonatal deaths than previously reported. Placenta Previa Placenta previa occurs when the placenta covers the cervix. In the past, the classification was made based on the relationship between the placenta and the cervical os, using terms such as total, partial, and marginal. With advances in transvaginal ultrasonography allowing for precise localization of the placental edge relative to the cervical os, these terms are being used less often. Instead, if any portion of the placenta overlies the os, it is referred to as a Previa, and any placenta near the os is termed low-lying. Placenta Previa Placenta Previa Placenta Previa – Epidemiology The incidence of placenta previa varies throughout the world but is estimated to be 1 in 200 pregnancies at term, corresponding to a prevalence of 4.0 per 1,000 births. The exact cause is unclear, but prior uterine trauma (scar from prior cesarean section) is a common finding. The placenta may implant in the scarred area, which typically includes the lower uterine segment. Conditions associated with placenta previa include (1) multiparity, (2) advanced maternal age, (3) smoking history, (4) male fetus, (5) previous cesarean delivery or other uterine surgery, and (5) previous placenta previa. Asian-American women are at increased risk for placenta previa compared with white women in the US. Placenta Previa – Epidemiology The presence of placenta previa increases the likelihood of (1) fetal anomalies, (2) neurodevelopmental delay, (3) sudden infant death syndrome, and (4) the risk that the mother will require a peripartum hysterectomy. Placenta Previa – Diagnosis Transvaginal ultrasonography is the “gold standard” for diagnosis of placenta previa. Measuring the distance from the placental edge to the internal os predicts the likelihood of antepartum hemorrhage and the need for cesarean delivery. The classic clinical sign of placenta previa is painless vaginal bleeding during the second or third trimester. All parturients with painless vaginal bleeding after 20 weeks gestation should be assumed to have placenta previa until proven otherwise. Digital or speculum examination should be avoided until ultrasonography excludes abnormal placentation. Placenta previa diagnosed in asymptomatic patients before the third trimester frequently resolves as pregnancy progresses. 90% of placentas identified as low lying in early pregnancy will normalize by the third trimester. Placenta Previa – Diagnosis The lack of abdominal pain and/or absence of abnormal uterine tone helps distinguish placenta previa from placental abruption. The absence of these factors does not exclude abruption, however, and patients with placenta previa are at risk for coexisting placental abruption. Placenta Previa – Obstetric Management Obstetric management is based on the severity of vaginal bleeding and the maturity and status of the fetus. Active labor, persistent bleeding, a mature fetus (gestational age of 36 weeks or greater), or nonreassuring fetal status should prompt delivery. The fetus is at risk from 2 distinct pathophysiologic processes (1) Progressive or sudden placental separation that causes uteroplacental insufficiency & (2) preterm delivery and its sequelae. The first episode of bleeding characteristically stops spontaneously and rarely causes maternal shock or fetal compromise. Expectant management in the hospital has been shown to prolong pregnancy by an average of 4 weeks after the initial bleeding episode. Placenta Previa – Obstetric Management Maternal vital signs are assessed frequently, and the hemoglobin concentration is checked at regular intervals. Fetal evaluation involves frequent performance of a non-stress test or biophysical profile and ultrasonographic assessment of fetal growth. Hemorrhage may be prevented by limitations on physical activity and avoidance of vaginal examinations and coitus, although the evidence supporting these measures is limited. Outpatient management has resulted in good outcomes in carefully selected patients. Outpatient management is reserved for stable patients without bleeding in the previous 48 hours who have both telephone access and the ability to be transported quickly to the hospital.  Placenta Previa – Obstetric Management In most cases of placenta previa diagnosed between 24- and 34 weeks gestation, a corticosteroid (betamethasone) is administered to accelerate fetal lung maturity. A significant number of patients with placenta previa have preterm labor, which may provoke bleeding. The use of tocolysis in women with placenta previa is controversial. Some Obstetricians may administer tocolytic therapy to decrease preterm uterine contractions to stabilize antepartum bleeding. Obstetricians must balance the potential cardiovascular consequences of tocolytic therapy in the event of maternal hemorrhage against the consequences of preterm delivery. Tocolytic therapy is not recommended for patients with uncontrolled hemorrhage or those in whom placental abruption is suspected.  Placenta Previa – Obstetric Management Fetuses of women with placenta previa may be at risk for other complications, including fetal growth restriction. Several factors may account for the association between placenta previa and fetal growth restriction: (1) the lower uterine segment may be less vascular than normal sites of placental implantation, (2) the placenta is often adherent to an area of fibrosis tissue, (3) patients with placenta previa have a higher incidence of first-trimester bleeding, which may promote a partial placental separation, reducing the surface area for placental exchange, and (4) although the blood loss from placenta previa is almost entirely maternal, trauma to the placenta with vaginal examination or coitus may result in some fetal blood loss, which could restrict fetal growth. Experts recommend that women with a placental edge-to-internal os distance greater than 1 cm be offered a trial of labor because the risk for antepartum hemorrhage and the need for cesarean delivery during labor are in this setting. Placenta Previa – Obstetric Management Parturients with a total previa, placental edge-to-internal os distance less than 1 cm, and/or significant bleeding will require abdominal delivery, as will some patients with nonreassuring fetal status.  Placenta Previa – Anesthetic Management All patients admitted with vaginal bleeding should be evaluated by an anesthesia provider on arrival. Volume resuscitation should be initiated using a non-dextrose-containing balanced salt solution. Women with placenta previa may remain hospitalized for some time before delivery, and at least one IV catheter should be maintained if bleeding is recurrent or imminent delivery is anticipated. Availability of cross-matched blood should be ensured. The American Association of Blood Banks (AABB) recommends repeating such tests every 3 days in pregnant women because of the small but finite risk of developing a new alloantibody during pregnancy. The use of lower-extremity sequential compression devices may decrease the risk of venous thromboembolism in patients on best rest. Pharmacologic prophylaxis may be withheld because of the risk for bleeding. Placenta Previa – Anesthetic Management The choice of anesthetic technique depends on the indication and urgency for delivery, the severity of maternal hypovolemia, and the obstetric history (prior cesarean delivery and risk for placenta accreta). An RCT comparing epidural with general anesthesia for cesarean delivery in women with placenta previa in the absence of active bleeding demonstrated that epidural anesthesia was associated with (1) more stable blood pressure after delivery and (2) lower transfusion rates and transfusion volumes with similar hematocrit measurements the day after surgery. Operative times, estimated blood loss, urine output, and APGAR scores were similar in the two groups. Combined spinal-epidural anesthesia, or even single-shot spinal anesthesia, is considered acceptable for patients without active bleeding. Placenta Previa – Anesthetic Management Patients who have placenta previa, even without active preoperative bleeding, remain at risk for increased intraoperative blood loss for three reasons. (1) The obstetrician may injure an anteriorly located placenta during uterine incision (2) After delivery, the lower uterine segment implantation site, lacking uterine muscle compared with the fundus, does not contract as well as the normal fundal implantation site. (3) A patient with placenta previa is at increased risk for placenta accreta, especially if there is a history of previous cesarean delivery. For these reasons, it may be advisable to place two large-bore IV catheters before the start of either elective or emergency cesarean delivery. No consensus exists on the need for blood product availability in these patients, but it seems prudent to order a blood type and screen and ensure blood product availability. If preoperative imaging indicates the possibility of a placenta accreta, preparation for massive blood loss should be undertaken. Placenta Previa – Anesthetic Management Risk for Placenta Accreta in % OF PATIENTS NUMBER OF PRIOR WITH PLACENTA Patients with Placenta Previa: CESAREAN DELIVERIES ACCRETA Relationship to number of prior 0 3 cesarean deliveries. 1 11 2 40 3 61 4 or more 67  Placenta Previa – Anesthetic Management Patients with placenta previa and active preoperative bleeding represent a significant challenge for the anesthesia care team. Frequently, such patients have just presented to the hospital and there is minimal time for evaluation. In these cases, patient evaluation, resuscitation, and preparation for operative delivery all proceed simultaneously. Because the placental site is the source of hemorrhage, the bleeding may continue unabated until the placenta is removed and the uterus contracts. Rapid-sequence induction of general anesthesia is the preferred technique for bleeding patients. The choice of intravenous induction agent depends on the degree of cardiovascular instability. In patients with severe hypovolemic shock, tracheal intubation may be accomplished without an induction agent, although this situation is rare.  Placenta Previa – Anesthetic Management The agent chosen for the maintenance of anesthesia depends on the maternal cardiovascular stability. In patients with modest bleeding and no fetal compromise, 50% nitrous oxide in oxygen can be administered with a low concentration of a volatile halogenated agent before delivery to prevent maternal awareness. The concentration of nitrous oxide or halogenated agent can be reduced or omitted in cases of severe maternal hemorrhage or fetal compromise. In these cases, a benzodiazepine such as midazolam can be administered to provide amnesia. Oxytocin should be administered by intravenous infusion immediately after delivery. The relatively amuscular lower uterine segment implantation site does not contract as efficiently as the uterine fundus. Placenta Previa – Anesthetic Management If bleeding continues, it may be best to discontinue the volatile halogenated agent completely after delivery and to substitute 70% nitrous oxide and an intravenous opioid or ketamine. These drugs, along with small doses of midazolam, can be administered without causing significant uterine relaxation or cardiovascular depression. A low-dose infusion of propofol and/or ketamine may be considered, with the caution that propofol causes decreased uterine contractility in a dose-dependent manner. If the placenta does not separate easily, placenta accreta may exist. In such cases, massive blood loss and the need for a cesarean hysterectomy should be anticipated. The need for invasive hemodynamic monitoring varies among patients. An indwelling arterial catheter is useful for patients with hemodynamic instability or for those who require frequent determination of hematocrit and blood gas measurements. Placental Abruption Placental abruption is defined as a complete or partial separation of the placenta from the decidua basalis before delivery of the fetus. Maternal hemorrhage may be revealed by vaginal bleeding or may be concealed behind the placenta. Fetal compromise occurs because of the loss of placental surface area for maternal- fetal exchange of oxygen and nutrients. Placenta l Abruptio n Placental Abruption - Epidemiology Placental abruption complicates 0.4% to 1.0% of pregnancies. The US incidence increased through the 1990s, particularly among African-American women, and then stabilized after 2000. The causes of abruption are not well understood, but several conditions are known risk factors for abruption. Conditions Associated with Placental Abruption Obstetric Conditions Maternal Comorbidities Trauma Advanced maternal age Hypertension Direct (blunt abdominal) Multiparity Acute or Chronic respiratory Indirect Preeclampsia illness (acceleration/deceleration Premature rupture of Substance abuse injury) membranes Maternal cocaine use Chorioamnionitis Maternal or paternal tobacco use Placental Abruption – Diagnosis The classic presentation of abruption consists of vaginal bleeding, uterine tenderness, and increased uterine activity, but not all symptoms are always present. In cases of concealed abruption, vaginal bleeding may be absent, and gross underestimation of maternal hypovolemia can occur. Bleeding may be painless. In some cases, abruption may manifest as idiopathic preterm labor. Patients may have a variety of nonreassuring fetal heart rate (FHR) patterns, including bradycardia, late or variable decelerations, and loss of variability. The diagnosis of placental abruption is primarily clinical, but in a subset of cases, ultrasonography may help confirm it. Ultrasonography is highly specific for placental abruption (96%), but it is not very sensitive (24%). Placental Abruption – Diagnosis Ultrasonography is also useful for determining placental location, which can exclude placenta previa as a cause of vaginal bleeding. The ultrasonographic examination can ascertain whether a retroplacental or subchorionic hematoma is present. Normal findings do not exclude the diagnosis of placental abruption. Placental Abruption – Pathophysiology Complications of placental abruption include hemorrhagic shock, coagulopathy, and fetal compromise or demise. 1/3 of coagulopathies in pregnancy are attributable to abruption, and coagulopathy is associated with fetal demise. Placental tissue displays tissue factor and other procoagulant substances on cell membranes, and it is surmised that when bleeding at the decidual-placental interface (abruption) occurs, these thromboplastic substances are released into the central circulation, resulting in consumptive coagulopathy and disseminated intravascular coagulation (DIC). Although some cases of abruption occur acutely (trauma), many abruptions complicate chronic, long-standing placental abnormalities. Investigators have noted strong associations between abruption, fetal growth restriction, and preeclampsia, and all three conditions share similar risk factors. Placental Abruption – Pathophysiology Histologic evidence of shallow trophoblastic invasion of the spiral arteries supports the conclusion that “ischemic placental disease” may underlie chronic placental hypoxia, leading to preeclampsia, fetal growth restriction, and abruption. The major risks for the fetus are hypoxia and prematurity. Separation of all or part of the placenta reduces gas exchange surface area and can lead to fetal death. The risk for intrauterine fetal demise increases as the detachment area increases, particularly when the location of bleeding is retroplacental rather than subchorionic. Inadequate transplacental oxygen exchange is exacerbated by maternal hypotension, which decreases uteroplacental blood flow. The increased perinatal mortality rate associated with placental abruption reflects both a high risk of fetal death and the consequences of preterm birth. Placental Abruption – Obstetric Management The definitive treatment is delivery of the infant and placenta, but the degree of maternal and fetal compromise and estimated gestational age determine the timing and route of delivery. If the fetus is at or near term and both maternal and fetal status are reassuring, vaginal delivery may be appropriate. If the patient is preterm, the extent of abruption is minimal, and the mother and fetus show no signs of compromise, the patient may be hospitalized, and the pregnancy allowed to continue to optimize fetal maturation. The obstetrician may administer a corticosteroid to promote fetal lung maturity. If the mother develops hemodynamic instability or coagulopathy, or the fetal status becomes nonreassuring, urgent cesarean delivery may become necessary. Vaginal delivery is preferred for patients with intrauterine fetal demise.  Placental Abruption – Anesthetic Management If abruption is suspected, the anesthesia provider should insert a large-bore IV catheter and assess hemoglobin, coagulation status, and blood product preparation. When gauging volume status, the clinician must remain aware of the possibility of hemorrhage concealed behind the placenta. The placement of a urethral catheter to monitor urine output may help assess the adequacy of renal perfusion. Placental Abruption – Anesthetic Management Labor and Vaginal Delivery Neuraxial labor analgesia may be offered in the setting of abruption provided that hypovolemia has been treated, and coagulation status is normal. The appropriateness of neuraxial analgesia with its accompanying sympathectomy in patients at risk for extension of abruption and further hemorrhage has been questioned; however, the risk that neuraxial analgesia will worsen hemorrhage- associated tachycardia and hypotension can be mitigated by appropriate intravascular volume replacement and use of vasopressors. A patient with abruption presenting for vaginal delivery may have a severe coagulopathy, particularly in the setting of fetal demise. In this case, intravenous patient-controlled opioid analgesia should be offered. Placental Abruption – Anesthetic Management Cesarean Delivery Spinal, CSE or epidural anesthesia may be administered in stable patients in whom intravascular volume status is adequate and coagulation studies are normal. General anesthesia is preferred for most cases of urgent cesarean delivery accompanied by unstable maternal status, a nonreassuring FHR pattern, or both. Propofol may precipitate severe hypotension in patients with unrecognized hypovolemia; ketamine and etomidate represent alternatives for patients with decreased intravascular volume. Aggressive volume resuscitation is critical. In cases of severe hemorrhage, insertion of an intra-arterial catheter may aid in prompt recognition of hypotension and allow for frequent blood sampling and assessment of anemia and coagulation status. Placental Abruption – Anesthetic Management Cesarean Delivery Patients with abruption are at risk for postpartum hemorrhage from uterine atony and coagulopathy; after delivery, oxytocin should be infused promptly. Persistent uterine atony requires the administration of other uterotonic drugs. Red blood cells and coagulation factors should be replaced as indicated by laboratory studies. Experts recommend aggressive monitoring and early replacement of coagulation factors, especially fibrinogen, to minimize the risk of developing coagulopathy. Most parturients recover quickly and completely after delivery. A minority of postpartum patients, notably those who have prolonged hypotension or coagulopathy, and who need massive blood volume and blood product replacement, are best monitored in a multidisciplinary intensive care unit. Uterine Rupture Rupture of the gravid uterus can be disastrous for both the mother and the fetus. Because of variations in nomenclature and severity, accurate determination of maternal and fetal morbidity secondary to uterine rupture is difficult. The most common variety of uterine scar disruption is separation or dehiscence; some cases are asymptomatic. Uterine scar dehiscence is defined as a uterine wall defect that does not result in excessive hemorrhage or FHR abnormalities and does not require emergency cesarean delivery or postpartum laparotomy. In contrast, uterine rupture, less common than dehiscence, refers to a uterine wall defect with maternal hemorrhage and/or fetal compromise sufficient to require emergency cesarean delivery or postpartum laparotomy. Uterine Rupture Uterine Rupture – Epidemiology Fortunately, uterine rupture occurs very rarely in women with an unscarred uterus, but it does occur. Previous uterine surgery (cesarean delivery or myomectomy) increases the risk, but the incidence of true uterine rupture after cesarean delivery is still low, occurring at a rate of less than 1%. Conditions associated with Uterine Obstetric Conditions Rupture Maternal Comorbidities Trauma Prior uterine surgery Connective tissue disorder Obstetric: Induction of labor forceps application/rotation High-dose oxytocin induction Internal podalic version Prostaglandin induction Excessive fundal pressure Grand multiparity (>5) Non-Obstetric: Morbidly adherent placenta Blunt Congenital uterine anomaly Penetrating Uterine Rupture – Epidemiology Although rupture of a previous uterine scar may occur in the absence of labor, it occurs more commonly during labor. Additional risk factors for uterine rupture during a trial of labor after cesarean (TOLAC) include (1) an inter-delivery interval of less than 12 to 16 months, (2) multiple previous cesarean deliveries, (3) post-term gestation, (4) maternal age older than 35 years, and (5) previous delivery with severe postpartum hemorrhage. Previous vaginal delivery and prior successful vaginal delivery after cesarean confers decreased rupture risk. Evidence of decreased lower uterine segment thickness on ultrasound examination increases rupture risk, but a precise clinically applicable threshold value below which a TOLAC should not be ordered has not been determined. Uterine Rupture – Epidemiology The rupture of a classical uterine incision scar (a vertical incision involving the muscular uterine fundus) is associated with greater morbidity and mortality than the rupture of a low transverse uterine incision scar because the anterior uterine wall is highly vascular and may include the area of placental implantation. The lateral extension of the rupture can involve the major uterine vessels and is typically associated with massive bleeding. Maternal death secondary to uterine rupture is rare. Rupture-associated neonatal hypoxic-ischemic encephalopathy or mortality occurs at rates of less than one per 1000 trials of labor after cesarean delivery in the US. Uterine Rupture – Diagnosis The variable presentation of uterine rupture may cause diagnostic difficulty. An FHR abnormality is the first sign of uterine rupture in more than 80% of patients. The triad of abdominal pain, abnormal FHR pattern, and vaginal bleeding is seen less frequently (9% of patients with rupture). Other presenting signs include vaginal bleeding, uterine hypertonia, cessation of labor, maternal hypotension, loss of the fetal station, decrease in cervical dilation, or a change in fetal presentation. Breakthrough pain and the need for frequent redosing during neuraxial labor analgesia may also indicate impending or evolving uterine rupture.  Uterine Rupture – Obstetric Management Treatment options for uterine rupture include repair of the uterus, arterial ligation, and hysterectomy. Uterine repair is appropriate for most cases of separation of a prior low transverse uterine scar and for some cases of rupture of a classical incision. However, the risk of rupture in a future pregnancy remains. A disadvantage of arterial ligation is that it may not control the bleeding and may delay definitive treatment. Hysterectomy may become necessary, albeit rarely.  Uterine Rupture – Anesthetic Management Patient evaluation and resuscitation are initiated while the patient is being prepared for emergency laparotomy. If rupture has occurred antepartum, fetal compromise is likely. General anesthesia may be necessary, but surgery can proceed under neuraxial anesthesia in stable patients with pre-existing epidural labor analgesia. Aggressive volume replacement is essential, and transfusion may be necessary. Urine output should be monitored. Focused cardiac ultrasound monitoring may be appropriate whenever there is uncertainty about the intravascular volume status. Vasa Previa Vasa previa occurs when the fetal blood vessels transverse the fetal membranes covering the internal cervical os. Consequently, the fetal vessels are not protected by the placenta or the umbilical cord, and rupture of membranes can be accompanied by tearing of a fetal vessel and exsanguination of the fetus. Two types of vasa previa exist (1) Type 1 – when the vessels are associated with a velamentous umbilical cord (2) Type 2 – when the vessels connect the lobes of a multilobed placenta or the placenta and a succenturiate lobe. Although no universal definition exists regarding the exact distance between fetal vessels and internal os that constitutes vasa previa, many clinicians use a threshold of 2 cm. This cutoff is based on a case series that demonstrated that all emergent deliveries caused by vasa previa had a fetal vessel within 2 cm of the cervical os. Vasa Previa Vasa Previa – Epidemiology Vasa previa occurs rarely (1 in 2500 to 1 in 5000 deliveries). Because it involves the loss of fetal blood, vasa previa is associated with a high fetal mortality rate (nearly 60% if vasa previa is unrecognized). The blood volume of the fetus at term is approximately 80 – 100 mL/kg. Therefore, the amount of blood that can be lost without leading to fetal death is small. In addition, the presence of vasa previa exposes the vulnerable fetal vessels to compression by the fetal presenting part, resulting in fetal hypoxia and death. Risk factors for vasa previa include (1) the presence of a velamentous cord insertion, (2) placenta previa or low-lying placenta in the second trimester, (3) placental accessory lobes, (4) in vitro fertilization, and (5) multiple gestation. Vasa Previa – Diagnosis Ultrasonography can be used to visualize the velamentous insertion of the vessels, but vasa previa should be suspected whenever bleeding occurs with the rupture of membranes, particularly if the rupture is accompanied by FHR decelerations or fetal bradycardia. Hemorrhage can also occur without rupture of membranes, making the diagnosis more difficult. Vasa Previa – Obstetric Management Prenatal diagnosis confers a neonatal survival benefit – neonatal mortality is 3% when vasa previa is diagnosed antenatally but increases to 56% when it is not. Any woman at risk for vasa previa should have an ultrasonographic examination with a transvaginal color doppler. The management of vasa previa is directed toward ensuring fetal survival. Timing of delivery reflects a balance between the risks associated with preterm delivery and the risk of vessel rupture if the pregnancy is allowed to continue. Experts advocate antenatal steroid administration between 30- and 32 weeks gestation to promote fetal lung maturity and hospitalization of the patient between 30- and 34 weeks gestation to ensure prompt delivery should rupture of membranes occur. Vasa Previa – Obstetric Management The best fetal outcomes will occur with elective delivery between 34- and 35-week gestation. Amniocentesis to evaluate fetal lung maturity is not recommended because delaying delivery is typically not an option. Ruptured vasa previa is a true obstetric emergency that requires immediate delivery of the fetus by cesarean delivery. Neonatal resuscitation requires attention to neonatal volume status.  Vasa Previa – Anesthetic Management The choice of anesthetic technique depends on the urgency of the cesarean delivery. In many cases, general anesthesia is necessary for prompt delivery. Postpartum Hemorrhage Conflicting definitions of postpartum hemorrhage exist; however, the most accepted definition is blood loss of more than 500 mL after vaginal delivery or more than 1,000 mL after cesarean delivery. ACOG defines hemorrhage as blood loss greater than or equal to 1,000 mL, or blood loss accompanied by signs or symptoms of hypovolemia within 24 hours of birth. Primary postpartum hemorrhage occurs during the first 24 hours, and secondary postpartum hemorrhage occurs between 24 hours and 6 weeks after delivery. Primary postpartum hemorrhage is more likely to result in maternal morbidity and mortality. Postpartum hemorrhage is the most common cause of maternal mortality worldwide and an important contributor to maternal death in the US. In the US, the current rate of postpartum hemorrahge is approximately 3%. Postpartum Hemorrhage Factors that may contribute to the rate of postpartum hemorrhage include (1) rising rates of obstetric interventions such as induction and augmentation of labor (2) increasing prevalence of obesity, multiple gestation, hypertensive diseases of pregnancy, and advanced maternal age. However, the rising prevalence of these risk factors does not entirely explain the upward trend in postpartum hemorrhage that has been observed. Postpartum Hemorrhage – Uterine Atony Epidemiology Uterine atony is the most common cause of severe postpartum hemorrhage, accounting for approximately 80% of cases; the incidence is increasing in the US. In addition to normal hemostatic mechanisms, postpartum hemostasis involves the release of endogenous uterotonic agents, primarily oxytocin and prostaglandins, that contract the uterus and constrict uterine vessels. Uterine atony represents a failure of this process. In addition, parturients with obstetric hemorrhage may have uterine arteries that are relatively unresponsive to vasoconstrictor substances. Postpartum Hemorrhage – Uterine Atony Epidemiology Conditions associated with Uterine Atony Obstetric Obstetric Maternal Other Management Conditions Comorbidities Cesarean delivery Multiple gestations Advanced maternal Tocolytic drugs Induced labor Macrosomia age High concentration of Augmented labor Polyhydramnios Hypertensive disease volatile halogenated High parity Diabetes anesthetic agent. Prolonged labor Precipitous labor Chorioamnionitis Postpartum Hemorrhage – Uterine Atony Postpartum Hemorrhage – Uterine Atony (diagnosis) An atonic, poorly contractile uterus and vaginal bleeding are the most common findings in patients with uterine atony. The absence of vaginal bleeding does not exclude this disorder because the atonic, engorged uterus may contain more than 1,000 mL of blood. Unrecognized bleeding may manifest initially as tachycardia; worsening hypovolemia eventually leads to hypotension. Postpartum Hemorrhage – Uterine Atony (management) Prophylaxis ACOG recommends active management of the 3rd stage of labor, including uterine massage and prophylactic oxytocin administration to decrease blood loss and transfusion requirements compared with expectant management. Oxytocin is the first-line drug for prophylaxis of uterine atony after delivery of a third- trimester pregnancy. (The number of high-affinity receptors for oxytocin increases greatly near term; alternative uterotonics are more effective in the first and second trimesters of pregnancy). Endogenous oxytocin is a nine-amino acid polypeptide produced in the posterior pituitary gland. The exogenous form of the drug (Pitocin, Syntocinon) is a synthetic preparation with a rapid onset and short half-life. Postpartum Hemorrhage – Uterine Atony (management) Prophylaxis Unfortunately, exogenous oxytocin can be associated with serious side effects, including vasodilation, tachycardia, hypotension, coronary vasoconstriction, myocardial ischemia, and rarely, even death, especially in hypovolemic or other hemodynamically compromised women. Many of these adverse effects are directly related to the dose of oxytocin. Administration of phenylephrine with oxytocin can mitigate the adverse hemodynamic consequences of oxytocin, but phenylephrine may not be necessary as long as an oxytocin bolus dose is avoided and the infusion rate is maintained below 1 unit/ minute, the threshold at which hemodynamic consequences become apparent. High doses of oxytocin administered concomitantly with large volumes of intravenous fluids, especially those containing free water, can lead to hyponatremia, seizures, and coma because of oxytocin’s structural similarities to vasopressin. Postpartum Hemorrhage – Uterine Atony (management) Treatment Despite preventive measures, postpartum uterine atony may occur. A multidisciplinary response to atony is imperative. General resuscitative measures include (1) additional large-bore IV access, (2) intravenous administration of crystalloid and colloid solutions and vasopressors, (3) laboratory determination of hemoglobin concentration or hematocrit and assessment of coagulation status, and (4) blood blank preparation of blood products for transfusion. Bimanual compression and massage of the uterus and continued infusion of oxytocin may help restore uterine tone. In the case of inadequate response to oxytocin, additional uterotonic agents should be employed. Three classes are currently available for the treatment of uterine atony: (1) oxytocin, (2) ergot alkaloids, and (3) prostaglandins. Postpartum Hemorrhage – Uterine Atony (management) Treatment The natural ergot alkaloids are produced by a fungus that commonly infests rye and other grains. Ergonovine and methylergonovine are the 2 ergot alkaloids currently available for use. Both are dispensed in ampules containing 0.2 mg. When administered via the IM route, they have a rapid onset, and the uterotonic effect usually lasts for 2 – 4 hours. Because ergot alkaloids rapidly produce tetanic uterine contractions, their use is restricted to the postpartum period. Postpartum Hemorrhage – Uterine Atony (management) Treatment Prostaglandins of the E and F families have gained wide acceptance as escalation therapy when high-dose oxytocin is inadequate. Concentrations of endogenous prostaglandins increase during labor, and levels peak at the time of placental separation. It is hypothesized that uterine atony may represent a failure of prostaglandin concentrations to increase during the third stage of labor in some women. 15-Metyhl prostaglandin F (Carboprost) & Misoprostol are the two common medications seen here. Postpartum Hemorrhage – Uterine Atony (management) Agent Dose/Route Relative C/I S.E. Notes Oxytocin 0.3 – 0.9 Units/min None Tachycardia Short duration of IV Hypotension effect Myocardial ischemia Free water retention Ergonovine 0.2 mg IM Hypertension N/V Long duration of Methylgonovine Preeclampsia Arteriolar constriction action CAD Hypertension May be repeated once after 30 min Methylprostaglandi 0..25 mg IM Reactive airway Fever May be repeated n disease Chills every 15 minutes up Pulmonary HTN N/V to 2 mg Hypoxia Bronchoconstriction Misoprostol 600 – 1000 None Fever Off label use micrograms PR, Chills sublingual, or N/V/D buccal Genital Trauma The most common childbirth injuries are lacerations and hematomas of the perineum, vagina, and cervix. Most injuries have minimal consequences, but some puerperal lacerations and hematomas are associated with significant hemorrhage, either immediate or delayed. Genital tract lacerations should be suspected in all patients who have vaginal bleeding despite a firm, contracted uterus. Retained Placenta Retained placenta is defined as failure to deliver the placenta completely within 30 minutes of delivery of the infant and occurs in approximately 3% of vaginal deliveries. Retained placenta typically results from 1 of 3 causes: (1) The placenta may be blocked behind a contracted lower uterus/cervix (incarcerated placenta). (2) The placenta may have adhered to the uterine wall (placenta adherens). (3) The placenta may be invading the myometrium (placenta accreta). The severity of bleeding ranges from minimal to severe and can be life-threatening and require transfusion. The risk for postpartum hemorrhage increases significantly if the interval between delivery of the infant and the placenta exceeds 30 minutes. Prophylactic oxytocin facilitates placental separation from the uterine wall, and, on balance, prophylactic oxytocin administered before delivery of the placenta is not associated with retained placenta after vaginal birth. Retained Placenta Risk factors for retained placenta include: History of retained placenta Preterm delivery Oxytocin use during labor Preeclampsia Nulliparity Retained Placenta Retained Placenta – Obstetric Management Treatment of retained placenta during the early postpartum period often involves gentle cord traction, uterine massage, manual removal, and inspection of the placenta. If manual extraction is not successful, curettage may be required. The clinician may need to discontinue oxytocin during curettage and then, once the placenta has fully delivered, restart it to augment uterine tone. The eventual removal of the placenta typically promotes uterine contraction and a reduction in bleeding, but close observation for evidence of recurrent hemorrhage is warranted. Because manual extraction of the placenta increases the risk of endometritis, the WHO recommends prophylactic antibiotic administration. Retained Placenta – Anesthetic Management Manual extraction of the placenta can be painful, requiring analgesia. In some cases, the administration of small amounts of sedatives and analgesics is adequate to allow examination and manual placental extraction by a skilled obstetrician. Administration of local anesthetic through an indwelling catheter, de novo neuraxial anesthesia may be considered in patients who are not bleeding severely and are hemodynamically stable. General anesthesia sometimes becomes necessary, particularly in hemodynamically unstable patients. In cases in which lower uterine or cervical contraction prevents placental passage, manual removal requires uterine relaxation. Historically, anesthesia providers performed rapid-sequence induction of general anesthesia, followed by the administration of a high dose of a volatile halogenated agent to relax the uterus. Retained Placenta – Anesthetic Management However, induction of general anesthesia in a parturient entails a risk of failed tracheal intubation, failed ventilation, and/or aspiration of gastric contents. Alternatively, nitroglycerin may be administered for uterine relaxation. Nitroglycerin provides a rapid onset of reliable smooth muscle relaxation and a short plasma half-life (2-3 minutes). Nitroglycerin most likely produces uterine smooth muscle relaxation by releasing nitric oxide, which temporarily decreases the patient’s systemic blood pressure. Uterine Inversion The turning inside-out of all or part of the uterus is a rare but potentially disastrous event. It is associated with severe postpartum hemorrhage, and hemodynamic instability may be worsened by concurrent vagal reflex-mediated bradycardia. The reported incidence of this disorder varies widely; recent reports suggest an incidence of approximately 1:3,400 deliveries. Risk factors for uterine inversion include (1) uterine atony, (2) a short umbilical cord, (3) uterine anomalies, (4) and overly aggressive management of the third stage of labor, including inappropriate fundal pressure or excessive umbilical cord traction. An abnormally implanted placenta (placenta accreta) may be first recognized when uterine inversion occurs. Uterine Inversion Uterine Inversion – Diagnosis Many cases of uterine inversion are obvious because of hemorrhage and a mass in the vagina, but others may not be readily apparent. Inversion should be suspected in all cases of postpartum hemorrhage. The ultrasonographic examination may show characteristic findings, such as an echo lucent zone within an echogenic mass filling the uterine cavity on transverse view. Historically, obstetricians have stated that the shock is out of proportion to the blood loss, but an underestimation of obstetric hemorrhage is more likely. Uterine Inversion – Obstetric Management Immediate replacement of the uterus, even before removal of the placenta, is the treatment goal, but it may be difficult to achieve. All uterotonic drugs should be discontinued immediately. The obstetrician should attempt to right the inversion by applying pressure through the vagina to the uterine fundus; ring forceps may be used on the cervix to apply counter traction. Insertion of an intrauterine balloon may prove useful during the treatment of uterine inversion, preventing reinversion. Uterine Inversion – Anesthetic Management Often, uterine tone precludes replacement of the uterus, and uterine relaxation is necessary for successful uterine reduction. The use of nitroglycerin to facilitate relaxation and replacement of the uterus has been reported. Fairly large intravenous doses (200 – 250 micrograms) may be required, and the anesthesia provider typically will need to support the circulation with IV fluids and vasopressors. Administration of general anesthesia with a volatile halogenated agent may become necessary, not only for uterine relaxation but also to prepare for laparotomy should it become necessary to correct the inversion. Once the uterus has been replaced, a firm, well-contracted uterus is desired. Oxytocin should be infused, and additional uterotonic drugs may be needed. Placenta Accreta Spectrum Placenta accreta is defined as a placenta that in whole or in part invades the uterine wall and is inseparable from it. Three types of placenta accreta (together referred to as placental accreta spectrum) occur. (1) Placenta accreta vera is defined as adherence of the basal plate of the placenta directly to uterine myometrium without an intervening decidual layer. (2) Placenta increta refers to a placenta in which chorionic villi invade the myometrium. (3) Placenta percreta represents invasion through the myometrium into serosa and sometimes into adjacent organs, most often the bladder. Placenta Accreta Spectrum Placenta Accreta Spectrum Placenta Accreta Spectrum Placenta Accreta Spectrum Placenta Accreta Spectrum – Epidemiology The increased incidence of placenta accreta mirrors the increased cesarean delivery rate, with a lag time of approximately 6 years. Previous cesarean delivery or other uterine surgery increases the risk of both placenta previa and placenta accreta. The combination of placenta previa with previous cesarean delivery synergistically increases the risk for coexisting placenta accreta, particularly if the placenta is anterior and overlies the uterine scar. Placenta previa with no prior uterine surgery conferred a 3% risk for placenta accreta. In women with placenta previa and one previous cesarean delivery, the risk for placenta accreta was 11%. In patients with placenta previa and a history of two previous cesarean deliveries, the incidence of placenta accreta increases to 40%. The incidence of placenta accreta was more than 60% in women with placenta previa and a history of three or more previous cesarean deliveries. Placenta Accreta Spectrum – Diagnosis In some cases of placenta accreta the condition is first suspected at vaginal delivery, when the obstetrician notes difficulty in separating the placenta from the uterine wall. The definitive diagnosis is then made at laparotomy. Antenatal diagnosis of placenta accreta facilitates effective planning. Antenatal diagnosis is associated with less maternal and neonatal morbidity, including decreased blood loss at delivery and transfusion of fewer units of blood products. Ultrasonography is a useful screening tool in patients with placenta previa and/or previous cesarean delivery and is the primary imaging modality used for making the diagnosis of placenta accreta. Placenta Accreta Spectrum – Obstetric Management ACOG advises that clinicians working at small hospitals without adequate blood bank supplies transfer patients with placenta accreta to a tertiary care facility because there is a predictable need for massive transfusion. Patients treated at institutions with a 24-hour in-house obstetrician and anesthesia provider, immediately available gynecologic oncologist, a fully stocked blood bank, and interventional radiologist services suffer less morbidity than those treated at hospitals without these services. Planned delivery with all of the necessary multidisciplinary collaborators present compared with emergency delivery is associated with less maternal morbidity, including fewer transfusions, complications, and intensive care unit admissions. However, circumstances may dictate emergency delivery, and institutions that manage women with suspected placenta accreta expectantly must have the capacity to mobilize the entire perioperative team at any time. Placenta Accreta Spectrum – Obstetric Management Some cases of vaginal bleeding remote from term resolve spontaneously, and expectant management may prolong the duration of pregnancy, at least into the third trimester. However, the risk for severe antenatal bleeding increases as gestational age increases. Timing of delivery, therefore, involves balancing this risk against the neonatal risks associated with preterm delivery. Decision analysis indicates that 34 weeks gestational age is the preferred time for planned delivery in most clinical circumstances involving the placenta and evidence of placenta accreta. Most patients with known placenta accreta should undergo planned preterm cesarean delivery and hysterectomy with the placenta left in situ because attempts to remove the placenta are likely to initiate hemorrhage. Because the positive predictive value of ultrasonography may be low, it is reasonable to await spontaneous placental delivery or even attempt manual extraction in cases in which the diagnosis is unclear, although manual extraction may increase the risk of bladder injury. Placenta Accreta Spectrum – Obstetric Management Preoperative placement of ureteral stents may minimize urinary tract injury. A midline vertical skin incision may provide optimal surgical exposure, and it may be necessary to modify the uterine incision to avoid cutting through the placenta. The preoperative insertion of internal iliac artery balloon catheters is controversial. Optimally, the balloons are inflated after delivery as a means to minimize blood in the surgical field and decrease blood loss and transfusion requirements. Cohort studies have reported conflicting data regarding the effects of balloon catheter placement on blood loss, transfusion requirements, and duration of the surgical procedure. Multiple complications can arise from the placement of these devices, some of them involving serious disruptions of the vasculature and lower extremity ischemia. Introduction of the arterial catheters, even without inflation, can cause fetal bradycardia, necessitating emergency delivery. Placenta Accreta Spectrum – Obstetric Management If employed, therefore, internal iliac artery balloon catheters should be placed in the operating room to avoid dislodgement during transport and to allow for rapid devilry should a fetal compromise occur. The Society for Maternal-Fetal Medicine (SMFM) recommends reserving the use of prophylactic intra-arterial balloon catheters for well-counseled women with a strong desire for fertility preservation, those who decline blood products and those with unresectable placenta percreta. Prophylactic use of resuscitative endovascular balloon occlusion of the aorta (REBOA) reduces blood loss during placenta accreta surgery, based on a meta-analysis of observational studies. Two forms of conservative therapy for placenta accreta have been described. In selected patients with a partial placenta accreta, small focal areas of placental invasion may be managed by curettage and oversewing. Alternatively, it may be possible to leave the intact placenta in situ, close the uterus and abdomen, and await spontaneous placental involution. Placenta Accreta Spectrum – Obstetric Management The ACOG considers planned peripartum hysterectomy to be the management of choice for patients with placenta accreta and cautions the obstetrician to reserve uterine conservation strategies for hemodynamically stable patients who strongly desire future fertility. Placenta Accreta Spectrum – Anesthetic Management Anesthetic management is similar to other cases of severe postpartum hemorrhage and peripartum hysterectomy. Preoperative suspicion for placental implantation abnormalities should alert the anesthesia provider to the potential for massive blood loss and transfusion. Initial blood loss may be minimal but can rapidly become torrential if the placental bed is disturbed or if the surgeons encounter unavoidable placental tissue during the hysterectomy. Invasive Treatment Options Regardless of the cause of obstetric hemorrhage, first-line conservative measures may fail to control bleeding. In these cases, invasive procedures must be performed promptly once delivery has occurred to avoid severe morbidity and mortality. Second-line options, including intrauterine balloon tamponade, uterine compression sutures, angiographic arterial embolization, and uterine artery and/or internal iliac artery ligation, may help to avoid hysterectomy. Unfortunately, no randomized controlled trails assessing the relative efficacy and safety of these options exist to guide management. In cases of intractable hemorrhage, hysterectomy may become necessary. Invasive Treatment Options – Intrauterine Balloon Tamponade Conservative method for controlling postpartum hemorrhage, especially when uterine atony or lower uterine segment bleeding is suspected. The technique can reduce rates of hysterectomy. An intrauterine balloon can be deployed quickly, requires minimal analgesia for both insertion and removal, and preserves fertility. Continued bleeding may be concealed behind the balloon. Failure may also be attributed to prolapse through a partially open cervix. In such cases, the balloon may be replaced and secured by applying bilateral ring forceps to the cervix or by placing a cervical cerclage. Few complications have been reported, although concerns for infection exist. Invasive Treatment Options – Intrauterine Balloon Tamponade Invasive Treatment Options – Uterine Compression Sutures Also referred to as B-Lynch suture Most useful in cases of refractory uterine atony but have also been used in cases of retained placenta and accreta. Estimated 92% success rate for this procedure. The suture may slip off of the uterine fundus and fail to provide compression. Placement of compression sutures may preserve fertility, but data on the long-term effects on fertility and pregnancy outcomes are lacking. Complications include (1) infection, (2) uterine necrosis, (3) and suture erosion. Invasive Treatment Options – Uterine Compression Sutures Invasive Treatment Options – Arterial Embolization Angiographic arterial embolization may be appropriate if moderate blood loss continues and if the patient is stable for transport to the interventional radiology suite. The uterine arteries, which are branches of the anterior trunk of the internal iliac arteries, provide the primary blood supply to the uterus. The ovarian and vaginal arteries also make a sizable contribution to uterine blood flow during pregnancy. During angiography, the radiologist can identify the vessels responsible for bleeding and embolize these vessels with gelatin sponge pledgets (gel foam). A small percentage of cases may require the placement of a metallic coil in addition to gelatin sponges. The gelatin sponge is a temporary occlusive agent, and flow through these vessels returns over time, preserving both the uterus and fertility. Invasive Treatment Options – Arterial Embolization Published success rates in emergently controlling postpartum hemorrhage with this approach vary between 70% and 100%. Successful treatment of acute postpartum hemorrhage with this modality requires rapid access to an angiography facility and a skilled interventional radiologist. The patient must be observed and monitored carefully while undergoing the procedure. Ischemic complications of embolization therapy have been reported, but the risk is reduced with the use of selective techniques. Invasive Treatment Options – Arterial Embolization Invasive Treatment Options – Surgical Ligation Bilateral surgical ligation of the uterine arteries may be used to control bleeding at laparotomy. In the case of failure to control bleeding, the surgeon may proceed with a more complex procedure that involves ligation of the tubo-ovarian and ascending and descending uterine arteries. Internal iliac artery ligation may also be considered, although it is more difficult to perform. Reported success rates are highly variable, and it appears that arterial ligation is being used less often than in the past. The rich collateral circulation of the uterus at term most likely contributes to failure to control bleeding, as does the challenging nature of the procedure itself. Engorgement of pelvic viscera, variability in vascular anatomy, and increased blood flow during pregnancy contribute to the risk for complications. Successful surgical ligation permits the preservation of fertility. Invasive Treatment Options – Surgical Ligation Invasive Treatment Options – Peripartum Hysterectomy Peripartum hysterectomy is the definitive treatment for postpartum hemorrhage unresponsive to medical and other invasive therapies. The two most common indications for this procedure are (1) Uterine Atony (2) Placenta Accreta The increase in hysterectomy for placental abnormalities is entirely explained by an increase in the cesarean delivery rate. Parturients with a history of previous cesarean delivery are more than five times as likely to require a peripartum hysterectomy as those without this history, and the risk for hysterectomy rises progressively with an increasing number of previous cesarean deliveries. Invasive Treatment Options – Peripartum Hysterectomy Peripartum hysterectomy is a technically challenging operation; the uterus is enlarged, exposure may be difficult, the vessels are engorged, and the pregnant uterus receives a rich collateral blood supply. The presence of dense adhesions from previous surgeries can further complicate the procedure. Compared with non-obstetric hysterectomy, patients undergoing obstetric hysterectomy are more likely to suffer postoperative hemorrhage and require a blood transfusion, have intraoperative urinary tract injury, and experience perioperative complications such as wound infection, venous thromboembolism, and cardiovascular and other medical complications. Mortality is more than 25 times higher in peripartum than in non-peripartum hysterectomy. Emergency peripartum hysterectomy is associated with increased blood loss, worse coagulopathy, and increased transfusion rates compared with planned peripartum hysterectomy. Invasive Treatment Options – Peripartum Hysterectomy Because of the challenging technical aspects of the procedure, the obstetrician may elect to perform a subtotal hysterectomy, wherein the cervix is left in situ. Subtotal approaches are associated with fewer urinary tract and other operative injuries and a shorter length of stay, but greater mean transfusion requirements and more frequent reoperation rates than total hysterectomy. Subtotal hysterectomy is not appropriate for patients with bleeding from the cervix, lower uterine segment, or both. Invasive Treatment Options – Manual Compression of the Aorta It can be a lifesaving procedure in the event of catastrophic obstetric hemorrhage. Effective aortic compression against a vertebral body in the upper abdomen should decrease blood flow to the pelvis, thereby allowing hemodynamic and hemostatic resuscitation and surgical control. An aortic cross-clamp requires vascular surgery expertise and retroperitoneal dissection but may be necessary to achieve hemostasis. Mild cardiac and renal dysfunction has been noted in non-obstetric patients if the aortic cross- clamp time exceeds 50 minutes. If a prolonged clamp time is required, the anesthesia provider should prepare for lactic acidosis and hypotension at the time the clamp is released. An endovascular aortic balloon may be inserted emergently via the femoral artery, and partial inflation just below the renal arteries may be sufficient to facilitate surgical visualization while preserving distal blood flow. Invasive Treatment Options – Manual Compression of the Aorta Anesthesia for Peripartum Hysterectomy Frequently challenging because massive blood loss may occur unpredictably. An experienced, skilled team is invaluable and critical to a successful outcome. Anesthesia providers may elect neuraxial anesthesia in a properly prepared patient. Intraperitoneal manipulation, dissection, and traction exceed similar maneuvers required with cesarean delivery alone. Maintenance of a T4 sensory level of anesthesia and judicious sedation may reduce the need for intraoperative conversion to general anesthesia. Longer surgical duration and a history of three or more prior cesarean deliveries increased the odds of requiring conversion to general anesthesia. Single-shot spinal anesthesia is unlikely to provide anesthesia of sufficient duration for an unanticipated hysterectomy. Patients who have delivered vaginally with pre-existing epidural labor analgesia may be managed successfully with the extension of the epidural blockade, but careful consideration of the hemodynamic status should precede the administration of local anesthetics into the epidural space. Anesthesia for Peripartum Hysterectomy Sympatholysis established before the onset of hemorrhage reduces excessive catecholamine response to blood loss and may improve survival. However, the induction of sympatholysis during hemorrhage may compromise end-organ perfusion and even precipitate cardiopulmonary arrest. As the magnitude of blood loss increases, general anesthesia becomes the anesthetic technique of choice. (1) Severely hypotensive patients may require tracheal intubation for airway protection. (2) Large fluid shifts and massive transfusion may adversely affect oxygenation so control of ventilation via an endotracheal tube becomes necessary. (3) The same fluid shifts increase airway edema, potentially making failed ventilation/intubation more likely as the surgery proceeds. (4) The massive transfusion of blood products often results in the need for the co-administration of potent vasopressors and calcium chloride, and thus, central venous access may be more easily accomplished. Anesthesia for Peripartum Hysterecto my Anesthesia for Peripartum Hysterectomy In all cases, patients at risk for peripartum hysterectomy managed with neuraxial anesthesia should be informed in advance that intraoperative discomfort or severe hemorrhage may mandate the intraoperative induction of general anesthesia. The induction of general anesthesia in the setting of severe hemorrhage may require the careful use of small doses of non-cardio depressant induction agents such as ketamine or etomidate. The circulation should be supported with the replacement of intravascular volume and vasopressors as needed. Regardless of the anesthesia technique used, two or more large-bore intravenous catheters should be inserted. Invasive blood pressure monitoring may aid in the prompt recognition of hypotension and provide access to frequent blood draws. Anesthesia for Peripartum Hysterectomy The blood bank should be alerted to the possible need for a massive transfusion. At least 4 units of PRBCS should be immediately available, with additional blood products, including plasma and cryoprecipitate, readily available without delay. ACOG recommends consideration of intraoperative blood salvage in cases with massive transfusion potential. Vasoactive drugs, fluid warmers, a forced-air body warmer, and equipment for rapid infusion of fluids and blood products should be accessible if the care team is anticipating the management of significant blood loss. Key Points Obstetric hemorrhage is the most common cause of maternal morbidity and mortality worldwide and a leading contributor to maternal mortality in developed nations. Most severe morbidity and mortality that occurs secondary to obstetric hemorrhage is considered preventable and caused by delays in recognition and treatment. The visual estimate of vaginal bleeding often underestimates true blood loss. Hypotension and tachycardia are late signs in hypovolemic shock. Antepartum hemorrhage usually represents a greater threat to the fetus than to the mother. Postpartum hemorrhage is increasing in both rate and severity in the developed world, mostly resulting from an increase in the incidence of uterine atony. Uterine atony is the most common cause of postpartum hemorrhage. The incidence of placenta accreta is increasing because of the higher cesarean delivery rate. Key Points Peripartum hysterectomy is increasing in frequency because of an increase in the incidence of both uterine atony and placenta accreta. Patients with placenta accreta are at high risk for massive hemorrhage and should be managed only in facilities with multidisciplinary specialists, including interventional radiologists and a well-staffed blood bank. Coagulopathy develops quickly during bleeding from the placental bed and may be out of proportion to blood loss or dilution because of the rapid consumption of fibrinogen. Intraoperative blood salvage may be lifesaving in cases of intractable hemorrhage if allogenic blood is not available; or if the patient refuses allogenic blood. Administration of TXA during postpartum hemorrhage decreases deaths caused by bleeding in low-resource settings. Its effect in high-resource settings is unknown, but it may decrease blood loss and transfusion risk.